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Beneficial effects of adiponectin on periodontal ligament cells under normal and regenerative conditions.

Nokhbehsaim M, Keser S, Nogueira AV, Cirelli JA, Jepsen S, Jäger A, Eick S, Deschner J - J Diabetes Res (2014)

Bottom Line: The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link.Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression.In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

View Article: PubMed Central - PubMed

Affiliation: Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany ; Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany.

ABSTRACT
Type 2 diabetes and obesity are increasing worldwide and linked to periodontitis, a chronic disease which is characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium. The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link. The aim of this in vitro study was to examine the effects of adiponectin on periodontal ligament (PDL) cells under normal and regenerative conditions, and to study the regulation of adiponectin and its receptors in these cells. Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression. The beneficial actions of enamel matrix derivative on a number of PDL cell functions critical for periodontal regeneration were partially enhanced by adiponectin. The periodontopathogen Porphyromonas gingivalis inhibited the adiponectin expression and stimulated the expression of its receptors. In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

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Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of TGFβ1, VEGF, POSTN, and RUNX2 at 1 d (a) and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of various concentrations of adiponectin (0.3, 1, and 3 μg/mL) on the mRNA expression of TGFβ1 and VEGF in the absence (c) and presence (d) of EMD at 1 d. Mean ± SEM (n = 9). Effects of EMD and/or adiponectin (1 μg/mL) on TGFβ1 (e) and VEGF (f) protein levels at 3 d. Unstimulated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of adiponectin (1 μg/mL) on the IL-6, IL-8, TNFα, and COX2 mRNA expressions at 1 d (g). Unstimulated cells were used as control. Mean ± SEM (n = 15); ∗significantly (P < 0.05) different from control.
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fig1: Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of TGFβ1, VEGF, POSTN, and RUNX2 at 1 d (a) and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of various concentrations of adiponectin (0.3, 1, and 3 μg/mL) on the mRNA expression of TGFβ1 and VEGF in the absence (c) and presence (d) of EMD at 1 d. Mean ± SEM (n = 9). Effects of EMD and/or adiponectin (1 μg/mL) on TGFβ1 (e) and VEGF (f) protein levels at 3 d. Unstimulated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of adiponectin (1 μg/mL) on the IL-6, IL-8, TNFα, and COX2 mRNA expressions at 1 d (g). Unstimulated cells were used as control. Mean ± SEM (n = 15); ∗significantly (P < 0.05) different from control.

Mentions: First we examined possible effects of adiponectin on the synthesis of molecules known to be involved in periodontal destruction and/or regeneration. As shown in Figure 1(a), adiponectin caused a significant upregulation of the TGFβ1, VEGF, and POSTN mRNA expressions at 1 d. A pronounced but insignificant upregulation was also observed for RUNX2 in adiponectin-treated cells at this time point. Adiponectin also led to a slight but significant increase in the POSTN mRNA expression at 3 d (Figure 1(b)). Interestingly, preincubation of cells with a specific inhibitor against the AMPK pathway inhibited the adiponectin-induced mRNA expression of TGFβ1, VEGF, POSTN, and RUNX2 by 62.85 ± 1.13%, 5.79 ± 1.89%, 42.27 ± 3.01, and 28.40 ± 2.17%, respectively, at 1 d.


Beneficial effects of adiponectin on periodontal ligament cells under normal and regenerative conditions.

Nokhbehsaim M, Keser S, Nogueira AV, Cirelli JA, Jepsen S, Jäger A, Eick S, Deschner J - J Diabetes Res (2014)

Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of TGFβ1, VEGF, POSTN, and RUNX2 at 1 d (a) and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of various concentrations of adiponectin (0.3, 1, and 3 μg/mL) on the mRNA expression of TGFβ1 and VEGF in the absence (c) and presence (d) of EMD at 1 d. Mean ± SEM (n = 9). Effects of EMD and/or adiponectin (1 μg/mL) on TGFβ1 (e) and VEGF (f) protein levels at 3 d. Unstimulated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of adiponectin (1 μg/mL) on the IL-6, IL-8, TNFα, and COX2 mRNA expressions at 1 d (g). Unstimulated cells were used as control. Mean ± SEM (n = 15); ∗significantly (P < 0.05) different from control.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4120919&req=5

fig1: Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of TGFβ1, VEGF, POSTN, and RUNX2 at 1 d (a) and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of various concentrations of adiponectin (0.3, 1, and 3 μg/mL) on the mRNA expression of TGFβ1 and VEGF in the absence (c) and presence (d) of EMD at 1 d. Mean ± SEM (n = 9). Effects of EMD and/or adiponectin (1 μg/mL) on TGFβ1 (e) and VEGF (f) protein levels at 3 d. Unstimulated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of adiponectin (1 μg/mL) on the IL-6, IL-8, TNFα, and COX2 mRNA expressions at 1 d (g). Unstimulated cells were used as control. Mean ± SEM (n = 15); ∗significantly (P < 0.05) different from control.
Mentions: First we examined possible effects of adiponectin on the synthesis of molecules known to be involved in periodontal destruction and/or regeneration. As shown in Figure 1(a), adiponectin caused a significant upregulation of the TGFβ1, VEGF, and POSTN mRNA expressions at 1 d. A pronounced but insignificant upregulation was also observed for RUNX2 in adiponectin-treated cells at this time point. Adiponectin also led to a slight but significant increase in the POSTN mRNA expression at 3 d (Figure 1(b)). Interestingly, preincubation of cells with a specific inhibitor against the AMPK pathway inhibited the adiponectin-induced mRNA expression of TGFβ1, VEGF, POSTN, and RUNX2 by 62.85 ± 1.13%, 5.79 ± 1.89%, 42.27 ± 3.01, and 28.40 ± 2.17%, respectively, at 1 d.

Bottom Line: The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link.Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression.In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

View Article: PubMed Central - PubMed

Affiliation: Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany ; Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany.

ABSTRACT
Type 2 diabetes and obesity are increasing worldwide and linked to periodontitis, a chronic disease which is characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium. The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link. The aim of this in vitro study was to examine the effects of adiponectin on periodontal ligament (PDL) cells under normal and regenerative conditions, and to study the regulation of adiponectin and its receptors in these cells. Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression. The beneficial actions of enamel matrix derivative on a number of PDL cell functions critical for periodontal regeneration were partially enhanced by adiponectin. The periodontopathogen Porphyromonas gingivalis inhibited the adiponectin expression and stimulated the expression of its receptors. In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

Show MeSH
Related in: MedlinePlus